Advancing Voice Research in a Rat Model: Investigating the Impact of Fiber Type Composition and Underlying Mechanisms of Atrophy in Rat Thyroarytenoid and Skeletal Muscles - Project Summary/Abstract Atrophy is complex and broadly defined as non-specific degradation of tissue and/or cells. Age-related skeletal muscle atrophy affects approximately 50 million people.1 Due to the increasing aged population, understanding mechanisms and treatment for muscle atrophy is a public health priority. In the vocal folds (VF)s, atrophy of the thyroarytenoid (TA) muscle is a commonly reported cause of dysphonia.2,3 The prevalence and etiology of TA atrophy are not yet fully understood, but can occur due to ageing4 and/or idiopathic/iatrogenic denervation5–11 yielding incomplete glottal closure, decreased maximum phonation time, and increased glottal airflow.12–14 Importantly, VF atrophy encompasses a multifaceted process that can involve the VF lamina propria and epithelium as well.15,16 In the absence of accessible human donor larynges, the rat has emerged as a surrogate to investigate TA physiology, including atrophy.6–10,17 However, the rat TA differs from human TA in fiber type composition.18 Specifically, the rat TA consists of nearly all type II fibers19 whereas the human TA consists of ~40% type I fibers and 60% type II fibers.20 The validity of rat models of TA structure and function is an area of debate, potentially leading to an incomplete understanding of critical biochemical processes. More importantly, treatment approaches for vocal fold atrophy are limited. This proposal will address this knowledge gap by comparing atrophic responses (i.e. aging and denervation) across other muscles with varying fiber type distributions to determine the relevance of fiber type on etiology of atrophy. These data will provide a foundation for a refined model with the ultimate goal of developing novel therapeutic strategies to assist the millions of patients with voice-related disabilities.
